Patients, family, friends, neighbors, even people we’ve just met ask us all sorts of questions about their health. Cholesterol levels are a common concern. For example, your brother calls to tell you that his LDL was high at his company health screening. “What does that mean?” he asks. “Should I be worried?”

Your own LDL cholesterol is 125, and your health care provider says it’s fine, but you’re confused. Your neighbor — same age, same gender, same provider — is about to start treatment to lower her LDL cholesterol to less than 100. “Why the difference?” she asks you.

Comparing numbers of total cholesterol and of “good” and “bad” cholesterol has become a regular topic of conversation among Americans. Yet, despite the public’s increased awareness of the link between cholesterol levels and heart disease, many people don’t comprehend the whole picture. Like your brother and your neighbor, they expect nurses to help them sort through what they hear from their health care providers, read in newspapers and magazines, or see on TV. As health educators and caregivers, nurses have a responsibility to understand the ups and downs of lipid profiles, the concept of global risk assessment, and the ways therapeutic lifestyle changes can improve health and decrease risk.

Panel discussion

Cholesterol and triglycerides are the two main lipids in blood. The body uses cholesterol, an essential component of all cell membranes, to form steroid hormones and bile acids. The liver produces most of the body’s cholesterol, but an estimated 20% to 40% comes from food sources.¹ Triglycerides are important in transferring energy from food into cells. To date, scientists cannot explain why lipids are also deposited in the arterial wall, causing atherosclerosis.²

The standard lipid panel, also called a lipoprotein profile, cardiac risk profile, or cholesterol profile, measures the total cholesterol, high-density lipoprotein cholesterol (HDL), and triglycerides, and calculates the low-density lipoprotein cholesterol (LDL). For accurate results, patients must fast for nine to 12 hours and avoid alcohol for 24 hours before the test. Food and alcohol can elevate the triglyceride level, distorting the interpretation of the panel. When levels are drawn from someone in a nonfasting state, only the total and HDL cholesterol values are accurate.

Other factors that can affect the accuracy of the lipid profile include acute illness, active weight loss, recent trauma, and pregnancy. The National Cholesterol Education Program (NCEP) recommends that all adults begin cholesterol testing at age 20, with repeat tests every five years or sooner, if clinically warranted.^2,3 If total cholesterol, LDL, or triglycerides are elevated, and/or the HDL is low, the care provider must rule out secondary causes of lipid abnormalities, such as diabetes, hypothyroidism, obesity, excessive alcohol use, liver disease, Cushing’s syndrome, obstructive liver disease, and renal disease. In addition, several medications can adversely affect lipids, including steroids, progestins, retenoids, thiazide diuretics, and beta blockers.²

Most nurses know that increased levels of total cholesterol and LDL are associated with increased coronary heart disease (CHD) risk. Criteria for CHD include a history of myocardial infarction (MI), angina (stable or unstable), and/or a history of revascularization procedures, such as coronary angioplasty. LDL cholesterol, referred to as bad (think of it as “lousy” cholesterol), carries most of the cholesterol in fasting serum. The higher the LDL, the greater the risk for CHD. HDL cholesterol (think good or “helpful” cholesterol) is made in the liver and intestines and believed to participate in reverse cholesterol transport, moving cholesterol away from the arterial wall.^1,3 The higher the HDL, the lower the risk of CHD. Another component of total cholesterol not routinely reported in the lipid panel is very low-density lipoprotein (VLDL), which consists mainly of triglycerides. VLDL particles transfer triglycerides to cells. Then, after losing enough triglyceride, the VLDL particles become LDL particles. Triglycerides are fat molecules in the blood. As an independent factor, elevated triglycerides are associated with increased risk of CHD. Total cholesterol is the sum of the LDL, HDL, and VLDL cholesterol.

The majority of patients with lipid abnormalities have hyperlipidemia, defined as high total and LDL cholesterol. Others have normal or near normal total and LDL cholesterol, but high triglycerides and low HDL. Thus, clinicians sometimes use the terms mixed hyperlipidemia, mixed dyslipidemia, or atherogenic dyslipidemia to describe these lipid disorders.^2,3 The key points to remember in reviewing the cholesterol panel are —

• The higher the total cholesterol and LDL levels, the higher risk for CHD.
• The higher the HDL, the more protective against CHD.
• High triglycerides are an independent risk factor for CHD.
• Low HDL is an independent predictor of CHD.

Who is at risk?

Although hyperlipidemia dominates the risk list, half of all coronary events occur in people without overt indicators of this condition.⁴ Other factors besides the lipid profile help a clinician assess an individual’s risk and determine treatment.

High Sensitivity C-Reactive Protein: Elevation of high sensitivity C-reactive protein (hs-CRP) is an independent risk marker for cardiovascular and peripheral vascular disease. The liver produces CRP, a general marker, in response to inflammation, and it is thought that inflammation plays an important role in cardiovascular disease. In a study of postmenopausal women, the hs-CRP level was the single best predictor of future heart attacks, even more predictive than high LDL.⁵ Both statin medications and aspirin lower hs-CRP. The blood test for hs-CRP is reasonably priced, and may be most helpful in guiding treatment when a patient has several risk factors, such as a strong family history of CHD, but normal or near normal lipid levels. Information about hs-CRP values can also help providers counsel patients of their risk if the patient is hesitant to be treated for known dyslipidemia.

Lipoprotein (a): Lipoprotein (a), known as Lp(a), is a lipoprotein subclass, consisting of an LDL particle to which apoprotein (a) is bound; apo(a) may interfere with thrombolysis. Epidemiologic evidence has linked elevation of Lp(a) with increased risk of CHD.³ In a study of almost 6,000 elderly U.S. citizens, Lp(a) elevation was linked to increased cardiovascular and total mortality risk in men, but not in women.⁴

Homocysteine: Measurement of homocysteine, an amino acid, is an expensive test. An elevated level correlates with premature development of MI, heart failure, stroke, and renal disease. While administration of folic acid, B6, and B12 vitamins lowers homocysteine levels, two recent trials have shown no effect on clinical outcomes. In fact, the patients in the active treatment group in the HOPE-2 trial had a 24% increased rate of hospitalization for unstable angina. Other studies are in progress, but current thinking is to not give B vitamins to lower homocysteine levels.^1,6

Metabolic Syndrome: Metabolic syndrome consists of moderate to high blood pressure (>130/85 mm Hg), impaired fasting glucose, now referred to as prediabetes (100 mg/dL to 125 mg/dL), central obesity (waist circumference >40 inches in men, >35 inches in women), low HDL (<40 mg/dL in men, <50 mg/dL in women), and high triglycerides (>150 mg/dL).³ Increased risk of coronary events at any level of LDL characterizes the syndrome. Often, those with metabolic syndrome have risk factors of obesity, sedentary lifestyle, and atherogenic diet.

Small, Dense LDL: The size and density of lipoproteins can affect the atherogenic effect. Elevated concentrations of small, dense LDL particles are associated with increased CHD risk, high triglycerides, and low HDL levels. Small, dense LDL is also associated with diabetes and insulin resistance syndrome.¹

Global risk assessment

Cholesterol levels and emerging risk factors are pieces to the puzzle that help predict a person’s risk of cardiovascular disease and determine who needs treatment for dyslipidemia. To prevent atherosclerosis, an advanced stage of cardiovascular disease, it makes sense to identify and treat those at risk before the lesions develop.³ To guide health care practitioners, the National Institutes of Health published the third report of the NCEP in May 2001, with revisions in 2004 based on newer studies. An expert panel reviewed major studies on lipid control and developed the evidence-based Adult Treatment Panel III (ATP III) guidelines.^7,8

Treatment recommendations target lowering elevated LDL as the primary goal of therapy. In deciding which patients to treat and how aggressively to treat, practitioners can follow these guidelines. The ATP III focuses on global risk assessment, which includes other risk factors beside lipid panel results. Following the guidelines, the practitioner adjusts the risk-reduction therapy to address the person’s absolute risk.⁷ Table 1 lists the ATP III classification of lipid values. Other risks fall into high, medium, and low categories. Those with a history of CHD or CHD risk equivalents are at highest risk for future CHD events. The risk equivalents include diabetes, peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease. Each of these conditions places the person at a 20% chance of suffering a CHD event over the following 10 years. For people in this high-risk category, the LDL goal is automatically set at <100 mg/dL without further assessment of risk. An optional goal of <70 mg/dL for LDL is now seen as a reasonable clinical strategy for these very high-risk patients. This is based on data from numerous clinical trials published between 2002 and 2004 that demonstrated further risk reduction with very low LDL levels. This optional goal of LDL <70 also applies to very high-risk people whose baseline LDL is <100. For moderately high-risk people with an LDL goal of <130, an optional goal of <100 is now a therapeutic option.⁸

Because of the accelerated atherosclerotic processes that occur in diabetics, diabetes is included as a CHD risk equivalent. In fact, someone with diabetes is as likely to suffer an MI as a person who has already had an initial MI. In addition, diabetics who have a coronary event have an unusually high death rate.⁷

Other risk factors besides LDL and CHD or a CHD-risk-equivalent history include —

• History of tobacco use, cigarette smoking
• Hypertension (blood pressure >140/90 mm Hg, or taking antihypertension medication)
• Low HDL (<40 mg/dL) associated with insulin resistance, elevated triglycerides, overweight/obesity, inactivity, type 2 diabetes, cigarette smoking, or high carbohydrate diet (60% of calories from carbohydrates)
• Family history of early CHD (first-degree male relative under age 55; first-degree female relative under age 65)
• Age — men age 45 and older; women age 55 and older

For people with two or more risk factors other than elevated LDL, the ATP III guidelines state that risk scores from the Framingham Heart Study are to be calculated to determine the risk of the individual’s chance of a CHD event in the following 10 years. One of the objectives of the ongoing Framingham Heart Study, which enrolled its first group of participants in 1948, was to identify the common factors or characteristics that contribute to cardiovascular disease. Over a long period of time, researchers followed a large group of participants who had not yet developed overt symptoms of cardiovascular disease or suffered a heart attack or stroke. Framingham risk scores incorporate the risk factors identified by the Framingham Heart Study as giving an individual higher risk if CHD.

In the ATP III assessment, a high HDL (>60 mg/dL) is considered protective, and a risk factor is subtracted. When 0-1 risk factors are present, Framingham scoring is not necessary because the 10-year risk of a coronary event is rarely high. However, clinicians may still choose to recommend treatment to patients with an excessively high LDL.⁷ Risk scoring tables are available at www.nhlbi.nih.gov/guidelines/cholesterol/index.htm.

The ATP III designates three risk categories that then determine LDL goals (see Table 2). The panel targets correction of the LDL as the primary goal of treatment, and clinicians can point to the risk categories to explain the basis of treatment to patients. The categories also help explain the variability of treatment plans from person to person, or for the same person from year to year. For example, an individual’s own health or family history may change form one year to the next.

Secondary targets of risk-reduction therapy, after controlling LDL, include metabolic syndrome, elevated triglycerides, and low HDL. High triglycerides continue to put a person at risk of cardiovascular disease, even if LDL is at goal. In people with very high triglycerides (200 mg/dL or higher), the ATP III sets non-HDL cholesterol, which is the total cholesterol minus the HDL, at 30 mg/dL higher than the person’s LDL goal as a secondary goal. In a patient with triglycerides less than 200 mg/dL after the LDL is at goal level, the clinician should calculate the non-LDL cholesterol. For example, if based on a Framingham risk assessment, a patient’s LDL goal is 100 mg/dL, but if the patient has very high triglycerides, the non-HDL goal (total cholesterol minus HDL) would be 130 mg/dL.⁶ If the non-HDL cholesterol remains above 130 mg/dL in this patient, further treatment is warranted, even if LDL is at goal.^7,8

Therapeutic lifestyle changes — first line approach

The two types of treatment for lipid disorders are therapeutic lifestyle changes, referred to as TLC by the ATP III guidelines, and medication therapy. (See part two of this self-study module for the section on medications.)

History, physical, and lab results in hand, the health care provider conducts a global risk assessment and draws up a treatment plan with the patient. The ATP III defines the TLC, which consist of general guidelines —

• Dietary changes: Decrease saturated fat to <7% of total calories, decrease dietary cholesterol to <200 mg/day.⁷
• Increase dietary intake of plant stanols and sterols to 2 to 3 g/day to further reduce LDL by 6% to 15%. Plant stanol and sterol structurally similar to cholesterol. They are derived from substances that occur naturally in plants. Incorporated into margarines, they help block the absorption of cholesterol in the intestine. In 2000, the FDA approved the health claim that Plant stanols and sterols reduce the risk of CHD.
• Eating soluble fiber, such as oat bran or psyllium (10 to 25 g/day), may reduce the LDL by 5% to 10%.^2,7
• Daily exercise of at least 30 minutes, or an energy expenditure of approximately 200 Kcal, to reduce LDL and increase HDL.⁷
• Weight reduction if overweight or obese.⁷

The nurse must work hand-in-glove with patient and family to incorporate the plan into the reality of their lives. Changes in eating habits and activity often seem daunting to some people. Referral to a registered dietician or qualified nutritionist can help ease the way.

Some might be confused by the fact that the TLC diet includes fat calories up to 25% to 35% of the total daily calories, but fat calories are divided into types of fats. Cholesterol intake is kept at less than 200 mg/day. Atherogenic fats, such as saturated fats, found in animal products, solid margarines, and palm and coconut oils, are kept low at less that 7% of daily calories; the same is true for intake of trans-fatty acids, found in hydrogenated or partially hydrogenated oils, often found in fried foods, cookies, and crackers. In 2003, the FDA published a final ruling requiring manufacturers to list trans-fatty acids on the nutritional labels.9 Monounsaturated fats, such as those found in olive oil, canola oil, nuts, and avocados, can account for up to 20% of the total daily calories, and polyunsaturated fats, such as those in other vegetable oils, for 10%. In those with metabolic syndrome, a higher intake of total fat, mostly in unsaturated fat, can actually help reduce triglycerides and raise HDL cholesterol.⁷ Smoking cessation is another way to reduce cardiovascular risk, and it can help raise a low HDL and decrease high triglycerides.^1,3

After six weeks of lifestyle changes, it’s time to reassess the lipid profile. If the patient has not reached the LDL goal, therapy to lower LDL must be stepped up. Specific dietary counseling can help, along with plant stanol/sterols or increased soluble dietary fiber.² Revisiting the importance of moderate but regular exercise may be necessary. If the patient’s LDL levels do not improve despite TLC, medication therapy is usually the next step.

Nonetheless, even when medication is indicated, TLC must remain front and center in the treatment of lipid disorders. With proper adherence to TLC, patients may lower their LDL an estimated 10% to 20% and increase HDL by 3% to 30%.³

As highly trusted professionals, nurses are in a key position to help others understand the concept of global risk assessment and the rich data supporting proper treatment to reduce CHD morbidity and mortality.